OBJECTIVETo investigate the effect of enteral nutrition(EN) on liver function and inflammatory response after abdominal operation in patients with liver dysfunction.

METHODSA prospective multicenter study was conducted. Patients requiring EN for at least 5 days after abdominal surgery with at least 1 abnormal liver function index were included. After operations, EN suspensions(TPF-FOS) were administered for 5 days after the return of bowel function with targeted content of 125.52 kJ(30 kcal)·kg(-1)·d(-1) maintained for a minimum of 3 days. Levels of serum pre-albumin, C-reaction protein(CRP), and liver function index were measured and the incidence of systemic inflammatory response syndrome(SIRS) was recorded before operation and 6 days after EN. Occurrence of gastrointestinal discomfort was monitored during the treatment.

RESULTSNo statistically significant difference was found in pre-albumin between preoperative level and post-EN level[(175.94±71.79) mg/L vs.(192.22±91.26) mg/L, P=0.162]. Patients with abnormal level of γ-glutamyl transpeptidase were less after EN compared to the preoperative period(30 vs. 40, P=0.041), as was total bilirubin (3 vs. 9, P=0.034). No significant differences in other indices of liver function were found. Total bilirubin and direct bilirubin decreased after EN support(P=0.000 and P=0.015, respectively). CRP was notably reduced after EN support [(48.74±65.16) mg/L vs.(25.79±23.63) mg/L, P=0.009] and the incidence of SIRS largely declined after EN support(19.0% vs. 10.3%, P=0.059). The incidence of gastrointestinal discomfort was 22.4% on postoperative day 1 and declined to 19.0% on postoperative day 5.

CONCLUSIONFor patients with liver dysfunction, enteral nutrition support with TPF-FOS after abdominal operation can reduce inflammatory response, improve liver function, and maintain serum protein level.

Abdomen ; surgery ; Adult ; Digestive System Surgical Procedures ; Enteral Nutrition ; Female ; Humans ; Inflammation ; therapy ; Liver ; physiopathology ; Liver Diseases ; complications ; physiopathology ; Male ; Middle Aged ; Postoperative Complications ; therapy ; Postoperative Period ; Prospective Studies

Objective: Brain and muscle ARNT-like protein 1 (BMAL1) is a core component of hepatocyte molecular clock and plays an important role in the regulation of other related rhythmic genes in the body through a transcriptional-translational feedback loop in molecular circadian oscillations. Therefore, the aim of this study was to investigate the role of BMAL1 in the rat periodontitis-induced liver injury. Methods: Twelve male Wistar rats were divided into the control group and the periodontitis group according to the random number table method. The rats in the control group were untreated. The periodontitis models were established by ligating the necks of the bilateral maxillary first molars in the periodontitis group rats. After 8 weeks, periodontal clinical indexes of rats in both groups were examined and executed. Micro-CT scans of the maxilla were performed and levels of the alveolar bone resorption were analyzed. Pathological changes in periodontal and liver tissue of rats in two groups were detected by HE and oil red O staining. Biochemical kits were used to detect glutamic-oxaloacetic transaminase (GOT), glutamic-pyruvic transaminase (GPT), total cholesterol (TC) and triglycerides (TG) in serum. The gene and protein expression levels of BMAL1, nuclear factor kappa-B (NF-κB) and tumor necrosis factor-α (TNF-α) in liver tissue were measured by real time fluorescent quantitative-PCR (qRT-PCR), immunohistochemistry (IHC) and Western blotting (WB) assays. Apoptosis was detected in liver tissues by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) kit staining. Results: The results of HE staining of maxillary first molars and micro-CT results of maxillary bones showed that alveolar bone resorption was significant in the periodontitis group of rats. The liver histopathology results showed infiltrated inflammatory cells in the liver tissue, disorganized liver cords and a large number of lipid droplets formed in the hepatocytes of the periodontitis group compared with the control group. The results of serum biochemical assay showed that the levels of GOT [(62.77±2.59) U/L], GPT [(47.54±1.04) U/L], TC [(3.19±0.23) mmol/L] and TG [(1.11±0.09) mmol/L] in the serum of rats with periodontitis were significantly higher than that in the control group respectively [GOT: (38.66±2.47) U/L, GPT: (31.48±1.57) U/L, TC: (1.60±0.05) mmol/L and TG: (0.61±0.09) mmol/L](P=0.003, P=0.001, P=0.002, P=0.038). qRT-PCR results showed that the mRNA expression level of BMAL1 was significantly decreased in liver tissue of the periodontitis group [(0.60±0.04)%] compared to the control group [(1.01±0.07)%] (t=4.80, P=0.009), while the mRNA expression levels of NF-κB and TNF-α [(1.62±0.12)%, (2.69±0.16)%] were significantly increased compared to the control group [(1.00±0.03)%, (1.03±0.16)%] (P=0.008, P=0.002); IHC results showed that the protein expression level of BMAL1 in liver tissue of the periodontitis group (averaged optical density, AOD) (11.58±2.15) was down-regulated compared to the control group (AOD) (22.66±1.67) (P=0.015), while NF-κB and TNF-α (AOD) (31.77±2.69, 24.31±2.32) were up-regulated compared to the control group (AOD) (19.40±1.82, 11.92±0.94) (P=0.019, P=0.008). WB results showed that the protein expression level of BMAL1 in liver tissue was down-regulated in the periodontitis group [(0.63±0.10)%] compared to the control group [(1.00±0.06)%] (t=3.19, P=0.033), while NF-κB and TNF-α [(1.61±0.12)%, (2.82±0.23)%] were up-regulated compared to the control group [(1.00±0.12)%, (1.00±0.11)%] (P=0.022, P=0.002). TUNEL staining showed increased apoptotic cells in the liver tissue of the periodontitis group of rats compared to the control group. Conclusions: Periodontitis may induce liver injury by down-regulating the BMAL1 expression levels in liver tissue, which in turn activates NF-κB signaling molecules, leading to the elevated levels of inflammation and apoptosis in rat liver.
Animals ; Male ; Rats ; Alanine Transaminase/metabolism* ; ARNTL Transcription Factors/metabolism* ; Aspartate Aminotransferases/metabolism* ; Biotin/metabolism* ; Bone Resorption ; Brain ; Chemical and Drug Induced Liver Injury, Chronic ; Cholesterol ; DNA Nucleotidylexotransferase/metabolism* ; Muscles/metabolism* ; NF-kappa B/metabolism* ; Periodontitis ; Rats, Wistar ; RNA, Messenger/metabolism* ; Triglycerides ; Tumor Necrosis Factor-alpha/metabolism*